Unit 3 - Motor Control Flashcards Preview

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Flashcards in Unit 3 - Motor Control Deck (71):

Upper motor neuron

Projects from cortical areas to spinal cord, synapses with lower motor neuron


Lower motor neurons

Motor neuron projecting from spinal cord to the motor end plate on muscle,
Synapses with upper motor neuron in ventral horn


Higher cortical areas

--> no direct contact with spinal cord, so influence = indirect.
ie: association cortex, basal ganglia, and cerebellum
(Signal via thalamus)


Spinal circuit reflex

Most simple motor circuit,
Sensory receptors --> spinal grey matter --> muscle
(Cutaneous, pain or muscle spindles)
ie: stretch reflex


Central pattern generator (CPG)

Moderately complex motor circuit;
Generated at brainstem or spinal cord,
INdependent of descending input, but turned on/off by cortex
Ex: walking or breathing


ballistic movement

rapid movement that MUST go to completion
(can't withdraw action once started)
ie: saccades (eyes), hemiballismus


organization of motor neurons in spinal cord

Medial: axial muscles -- control balance/stability
Lateral: distal muscles -- fine motor control
dorsal: flexor mm.
ventral: extensor, mm.


motor unit

a single alpha motor neuron, along with all muscle fibers innervated by it (3-1,000)
-- small size = fine motor control
* increase muscle force by recruiting motor units


2 types of alpha motor neurons (+ function)

"red" (small): slow, low force, fatigue-resistant
"pale" (large): fast, fatiguable


monosynaptic/myotactic reflex

1. passive stretch of tendon
2.a) contract muscle (via muscle spindle Rs)
b) relax opposing muscle ("reciprocal inhibition")


nocioceptive withdrawal reflex

1. nocioRs sense pain (ie: step on tack)
(--> Lissauer's tract)
2. a) ipsilateral flexor contracts
b) contralateral extensor contracts
* provides support for opp. limb to "escape"


Muscle proprioceptive pathway

1. muscle spindle (stretch R)
2. ipsilateral dorsal column - spinal cord
3. dorsal column nucleus
* decussate!*
4. contralateral medial lemmniscus
5. VPL of thalamus --> S1 (cortex)


muscle spindle

in parallel with mm., w/ stretch Rs;
--> passive stretch/increase muscle length
- 1a and II axons
** gamma mns change length to increase sensitivity (via intrafusal fibers)
* stimulated by vibration (lengthening illusion)*


Golgi tendon

in series w/ mm (at end, inside collagen);
--> isometric contraction (tension on muscle)
- 1b axons to inhib. interneurons, compensate for fatigue


Lesion to posterior parietal cortex

1. apraxia (loss of learned/skilled movements)
2. optic ataxia (mis-reaching)


Lesion to premotor/supplementary motor cortex

poor planning and sequencing,
decreased spatial organization
* feet = medial, head = lateral


lesion to basal ganglia

1. akinesia/bradykinesia (slowed mvmt)
2. ballismus
(responsible for selection and initiation of mvmt)


lesion to cerebellum

ataxia (uncoordinated mvmt)
* normally responsible for mvmt smoothness and coordination


Cortical circuits involved in voluntary movement

Direct to spinal neurons:
1. corticospinal tract; 2. corticobulbar (*bilateral!)
INdirect to spinal neurons:
1. corticorubral tract; 2. corticoreticular tract


Thalamic motor control

1. VPL = somatosensory (proprioceptive/cutaneous info)
2. VA/VL = timing/coordination


Major cortical motor areas

1.Primary motor cortex (BA 8)
2. Supplementary motor cortex (BA 6)
3. Premotor cortex (BA 6)
4. Cingulate Motor area (BA 24)
Req's: thin granular layer (IV), & electrical stim. to area --> mvmt


Neurons in primary motor cortex (M1)

each = directionally tuned,
fire: just before & during mvmt, (latency = 100-150 ms)
* population vector of neurons matches direction of mvmt*
-- increase firing rate = increase force


lesion to pyramidal tract

decrease in hand control, ie:
1. thumb-finger opposition
2. precise grip (=> "scoop hand")
3. single digit extension


lesion to primary motor cortex

--> spastic paresis (bc = upper motor neurons)
- lose fine motor control
- increase tone/hyper-reflexia
* adjacent representations fill in void! (modified by use/experience)


Function of Premotor cortex (BA 6)

#1) learned visual stimulus-response associations
2) rule-based actions
3) motor planning (to instructional cue)
* ventral (PMv) = hand grasp & mirror neurons
* dorsal (PMd) = arm reach


Supplementary motor area function (SMA):

self-initiated mvmts, mental mvmt rehearsal, and learned motor sequences.
* single neurons = selective for specific mvmt sequences (Bop-it);
--- "bereitshift potential" = from EEG over SMA.


"distributed processing" for motor cortex:

Multiple distinct cortical areas responsible for motor processing,
* all areas have different but overlapping function*
--> damage to 1 area = mild/transient,
BUT damage to >1 area = severe, persistant


input to inferior cerebellar peduncle:

1. vestibular nuclei
2. brainstem
3. spinal cord
* output = vestibular nuclei


input to Middle Cerebellar Peduncle:

1. Pontine Relay Nuclei
2. Cerebral cortex
(output = cerebellum)


Cellular organization of the cerebellum

3 layers, 5 total cell types.
1. Purkinje layer: 1 cell thick (purkinje cell bodies)
2. Molecular layer: purkinje dendrites, parallel fibers, and interneurons
3. Granular layer: granule cells (= cell bodies of parallel fibers),
* inhibited by Golgi cells (interneurons, NT = GABA)


synapses on Purkinje cells

all use glutamate as excitatory NT,
1. Climbing fibers (from Inf. Olive) --> short AP burst
= motor error signal (teaching)
2. Granule cells (become parallel fibers) --> single AP
= sensory feedback/motor commands
*** Purkinje cells = INhibitory to Deep Cerebellar Nuclei ***


Climbing fibers

neurons connecting Inferior Olive to Purkinje Cells (excitatory),
for signaling motor errors;
input to Inf.O. from:
Cerebral cortex, Red Nucl., Spinal Cord, Deep Cerebellar Nuclei


Mossy Fibers

neurons in cerebellum connecting input to Purkinje cells (excit.),
via Granule cells/parallel fibers.
Input from: Cerebral cortex, Brainstem and Spinal cord.


Long-term Depression

phenomenon where parallel fiber signaling is weakened by simultaneous firing of climbing fibers.


Output from cerebellum

info from cerebellum to a) motor thalamus, b) Red Nucleus
via Superior Cerebellar Peduncle.


Inferior Olive (relation to cerebellum)

Receives input from Cortex, Red Nucleus, Spinal Cord, and Deep Cerebellar Nuclei ("Loop Circuit").
* sends to CONTRAlateral cerebellar hemisphere.
Inferior Olive --> Climbing Fibers --> Purkinje Cell(s)


unilateral lesions in cerebellum cause...

Hypotonia (if decrease gamma motor neuron activity via thalamus),
= IPsilateral deficits bc cross twice (in SCP and after M1)



= vermis and flocculonodular lobe.
controls balance and eye mvmts,
Inputs: vestibular nuclei, visual cortex, motor cortex (for posture)
Output: Vestibular nucleus
Lesion deficits:
- balance: fall to side of lesion,
- Eyes: spontaneous nystagmus, poor smooth pursuit (eyes(



= vermis and medial hemispheres;
Receives somatosensory info.
Input: spinal cord (ipsilateral limb tracts)
Output: to Reticular Formation (via Fastigial nucleus)
Lesion Deficits:
Ataxia, dysmetria (poor coordination), hypotonia, tremor, poor rapid alt. mvmts/decomposed mvmt.



= lateral hemisphere; helps w/ voluntary mvmt.
Input: Motor cortex, somatosensory cortex, Association cortex
Output: Motor thalamus (via dentate nucleus)
Lesion Deficits: fine mvmt ataxia, cognitive deficits


Basal Ganglia

"Gates" mvmt (selection and initiation); somatotopic organization.
= Striatum, Globus Pallidus, Subthalamic nucl, and Substancia Nigra.
-- Direct Path: suppress inhibition --> increase motor output.
--- Indirect: inhibit direct path --> decrease motor output.


lesion to caudate nucleus

deficit = robotic walking


Lesion to putamen

deficit = vulgar and impulsive personality shift, hypersexuality


striatum neurons

= medium spiny neurons ("MSNs") --> inhibitory projections to globus pallidus, NT = GABA.
(+ some interneurons)
* somatotopic organization


Nigrostriatal pathway

from STN (subthalamic nucleus) to Striatum;
D1 Rs: + to MSNs in Direct path.
D2 Rs: - to MSNs in INdirect path
==> promote movement (aka motor output)
** Dopamine deficit in Parkinson's limits this pathway.


Parkinson's Disease

--> akinesia, bradykinesia, slow rest tremor
= Dopamine deficit to nigrostriatal pathway,
From oxidative stress, mimicked by MTPT drug.
Treatment: L-DOPA, Pallidotomy (decrease inhibitory GPi output), DeepBrain Stimulation


Huntington's Disease

autosomal dominant mutation (CAG repeat on chrom.4 short arm)
-> MSNs and cerebral cortical neurons die
==> chorea, athetosis (slow writing), Dementia, and personality changes.
* 30-50 yr. onset


Direct Basal ganglia pathway

Cortex --> (+) striatum --I (-) GPi/SNr -/-I Thalamus
==> suppress inhibition = increase motor output


INdirect Basal Ganglia pathway

Cortex--> striatum--I GPe -/-I (-)STN --> (+)GPi/SNr --I Thalamus
==> inhibit direct pathway = Decrease motor output


Lesion to Globus pallidus

--> dystonia (sustained muscle contractions, abnormal postures, etc.)


lesion to Subthalamic Nucleus (STN)

--> hemiballismus (involuntary flinging motion in extremities)
bc lesion causes LOSS in mvmt inhibition (via INdirect pathway)


Muscle groups used for postural tone

(tonic activity in muscles opposing gravity)
- Upper limb flexors
- Lower limb extensors


2 routes for postural control

1. Direct: via vestibulospinal tract to alpha mns
2. Reflex Route: via corticospinal or reticulospinal tracts to gamma mns
==> act on muscle spindles to increase tone via alpha mns


Reticulospinal tract and postural control:

to modulate gamma mns --> affect alpha mns;
a) Cortex --I Pontine Reticular Formation --> + gamma mns
= increase m. tone.
b) Cortex --> Medullary Reticular Formation --I - gamma mns
= DEcrease tone.


Lesion to "MRF" (medullary reticular formation):

INcreased tone bc DISinhibit gamma neurons
(so increase alpha mn work too)


Median Vestibular tract ("MST")

carries bilateral cervical information from semicircular ducts,
=> stabilize head position, influence alpha mns to neck muscles.
(maintain center of gravity)


Lateral Vestibular tract (LVST)

ipsilateral to all levels of spinal cord,
=> stabilize stance/maintain balance and posture.
to alpha mns of legs
(anti-gravity and tilt reflexes)


Lesion to vestibulospinal tracts

loss of balance,
will fall towards side of lesion



lesion above the red nucleus, so red nuc = DISinhibited;
(ie: cerebral cortex, internal capsule, thalamus)
Sx --> flex arms and extend legs



lesion below the red nucleus, disrupts the rubrospinal tract
(loss of tonic input from cortex --> hyperactive stretch reflex)
-> increase gamma mn activity = increase postural tone
Sx --> extend arms and legs, arch head back
Treatment: cut dorsal roots to decrease rigidity


Reasons for return of sensation >2 months after lesion
(to descending systems)

--> hyperactive reflexes and hypertonic bc...
1. denervation sensitivity (increase sensitivity to input)
2. synaptic void filled by nearby neurons (increase strength of proximal circuits)



ballistic mvmt to rapidly redirect fovea,
*not modifiable once started, = CPG reflex.
** CAN perform on verbal command**
During mvmt: blurry image and no f(x)al vision
Latency: 150-200 ms, Duration: 20-50 ms
Velocity: ~400 degrees/second


Smooth pursuit (eye mvmt)

eye mvmt to follow moving target -- eyes match speed of target;
*"retinal slip" = speed mismatch
* canNOT perform on visual command (uses saccadic tracking)*
DO have f(x)al vision while move eyes
= voluntary cortical modulation of reflex mech in brainstem


Lesion to cortical eye fields and/or brainstem visual centers

1 or other: mild, transient saccade deficits

Both areas: severe and persistent saccade deficits


Cortical eye fields

code direction and amplitude of eye movement,
each neuron = directionally tuned.
= frontal/supplementary eye fields and lateral intraparietal area;
*project to: a) brainstem (saccade reflex)
b) pontine relay nuclei/cerebellum (smooth pursuit)


Superior colliculus

1 of 2 visual centers in brainstem, = on tectum of midbrain;
F(x): reflexive, contralateral saccades
- superficial layer: stimulus position
- deep layer: direction/amplitude of saccade


reticular formation

1 of 2 visual centers in brainstem,
= saccade central pattern generator
a) midbrain (riMLF) = vertical component
- output: abducens nucleus
b) pons (PPRF) = horizontal component
- output: occulomotor nucleus
*output goes 1st to nucleus of IPsilateral eye!


"Pulse-step" pattern for visual saccades

= firing pattern in abducens and occulomotor nuclei;
1. pulse: burst --> saccade
2. step: tonic activity --> fixation/tension


pathway for smooth pursuit:

1. cortical eye fields/extrastriate visual cortex
- via Pontine Relay Nuclei -
2. Cerebellum: Flocculum
3. Vestibular nuclei
4. Brainstem nuclei (direct to abducens, INdirect to occulomotor)
5. Eye muscles


Function of Vermis (cerebellum) in saccades

adjusts amplitude of saccade to match target
(so gaze lands accurately on target)
*Lesion ==> dysmetric saccades (miss/overshoot target)


Lesion to flocculum (cerebellum)

--> smooth pursuit = abolished!
but saccades not affected.
(so use saccadic tracking to overcome deficit)